Parasites pt 2 Toxoplasmosis - Leishmaniasis Flashcards
Toxoplasma gondii: transmission
ingestion of oocysts in raw pork
inhalation of oocysts
inhalation of oocysts from cat feces
congenital: if a pregnant women is exposed to taxoplasma for the very first time, because she hasnt produced antibodies. she can pass to fetus. TORCHS
Toxoplasma gondii: morphology
oocysts is infectious
trophozoites
toxoplasma gondii: clinical findings
congenitally aquired (Torches)
results in still birth or live birth with symptoms early or later.
immunocompromised patietns disseminated infection with may include: encephalitis presenting as a brain mass. chorioetinitis. hepatosplenomegaly+lymphadenopathy
pneumonia
outcomes for child acquiring Toxoplasmosis transplacentally
chorioretinitis, blindness, seizures, mental retardation, microcephaly.
normal children may develop reactivation in adolescents– can lead to blindness.
Dignosis of Toxoplasmosis gondii
serology: high IgM and IgG
radiology: CT scan showing contrast enhancing mass in the brain
examination of the retina revealing retinal inflammation
what kind of microbe of T. gondii?
obligate intracellular parasites
Pneumocystis carinii: transmission
acquired early age via respiratory route. remains latent in normal host.
85% of children have had exposure asymptomatically. lives comfortably in people with intact immune systems. in AIDS and immunocompromised patients, it can multiply in the lungs and cause severe interstitial pneumonia
Penumocystis carinii: morphology
flying saucer appearing fungus in alveolar lung secretions (sputum samples)
pneumocystitis carinii: clinical findings
PCP interstitital pneumonia: fever, dry/unproductive cough. Most common opportunistic infection in patients with AIDS. 15% change of infection/year in AIDs patients. 80% lifetime risk without prophylactic therapy.
Pneumocystitis carinii: diagnosis
silver staining
flying saucer appearing fungi in saline induced sputum
brconhoalveolar lavage with bronchoscope. bronchial wall biopsy with bronchoscope. X-ray: find an interstitial pneumonia with diffuse infiltrates.
when are aids patients susceptible to pneumocystis carinii?
when their CD4 count is less than 200.
Plasmodium falciparum: episodes of chills and fevers
continuous
Plasmodium falciparum: continual reproduction in the liver?
no
Plasmodium falciparum: anemia?
yes
Plasmodium falciparum: sever clinical manifestations?
yes: brain and kidney
Plasmodium falciparum: chloroquine sensitivity?
no except in central america
Plasmodium vivax and ovale: episodes of fever and chills?
at 48 hr intervals
Plasmodium vivax and ovale: continual reproduction in the liver?
yes!!!!!!!
Plasmodium vivax and ovale: anemia?
yes
Plasmodium vivax and ovale: severe clinical manifestations
no
Plasmodium Malariae: fever and chills?
every 72 hrs
Plasmodium Malariae: continual reproduction in the liver?
no
Plasmodium Malariae: anemia?
yes
Plasmodium Malariae: severe clinical manifestations?
no
Plasmodium knowlesi: chills and fever?
not know
Plasmodium knowlesi: continual reproduction in the liver?
no
Plasmodium knowlesi: anemia?
yes
Plasmodium knowlesi: severe clinical manifestations
yes
plasmodium: transmission
anopheles mosquito
plasmodium: morphology
several forms in life cycle. “hypnozoite stage” dormain form that hangs out in the liver
plasmodium: clinical findings: vivax and ovale
every 48 hrs –> chills/fevers “tertian malaria”
hepatosplenomegaly caused by “duffy a” and “b” antigens
plasmodium: clinical finding: Malariae
Quartan malaria: sweating/chills/fever every 72 hrs.
Diagnosis of Plasmodium
blood smears: trophozoites “diamind ring shape”
Babesia Microti: transmission
ixodes scapularis, the tick
babesia microti: morphology
sporozoites from tick cause infection
sporozoites mature into trophozoites in humans and infect the RBCs
babesia microti: clinical findings
immunocompetent ppl: asymptomatic
immunocompromised ppl: anemia due to hemolysis, fatigue, and protracted course
babesia microti: diagnosis
blood smear, PCR, serology
“classic maltese cross” on blood smear. patients may be co infected with lyme disease
Leishmania: mode of tranmission
sandfly bite, contaminated blood transfusion, zoonotic: carried by rodents, dogs, foxes.
LEishmania: morphology
Promastigote: flagellated (inside the sandfly).
Amastigote: instracellular and nonflagellated (inside phagocytic cells of reticuloendothelial systems.
Leishmania: clinical findings
cutaneous leishmaniasis- single ulcer at site of sandfly bite (oriental sore).
diffuse cutaneous: nodules at bite site (which do not ulcerate, especially near nose. can last up to 20 yrs without treatment
mucocutaneous: ulcers appear on mucous membranes after first ulcer at bite site heals. ulcers erode the nasal septum, soft palate, and lips. can last 20-40 ys.
visceral: leishmaniasis (kala-azar): comon in young, malnourished children. fever, anorexia, weight loss, and abdominal swelling from hepatomegalgy and massive splenomegaly. often fatal.
which Leishmania has massive splenomegaly?
L. Donovani
In whom will diffuse cutaneous leighmaniasis occur?
ppl with immunocompromised situations, malnurished ppl etc
because they dont have cell mediated immune response, L. skin test is negative
how is a diagnosis of leishmaniasis made with those exhibiting mucocutaneous and cutaneous lesions?
mucocutaneous: skin scrapings
cutaneous: Leishmania skin test. cell mediated immunity
Trypanosoma rhodesiense/gambiense: tranmission
TseTse fly. Following bite, flagellated form of these two organisms called Tryptomastigote spread via persons bloodstrewam to LNs and CNS
Trypanosoma R/G: clinical manifestations
red painful skin ulcer that heals within 2 weeks. Systemic spread–> fever, headaches, dizziness and LN swelling. –> fever abates –> fever resumes –> fever abates .
CNS symptoms develop, drowsiness in the daytime, sleeping sickness) behavior changes, difficulty with walking, slurred speech, finally coma and death.
what’s the big “pattern” in African sleeping sickness?
intermittent fevers followed by CNS problems, sleepiness, ataxia, slurred speech, coma and death.
T. Brucei Gambiense is also called
West African Sleeping sickness
notable for slowly proressing fevers, wasting, late neuro symptoms.
T. brucei rhodesiense is also called
East African Sleeping sickness. similar to west african variety but more severe. death occurs within weeks to months. rapid progression from recurrent fevers to early neurologic disease
Amastigotes
rounded cells without flagella (both trypanosoma and leishmania)
promastigotes, epimastiogtes, tryppmastigotes
flagellated motile forms (both trypanosoma and leishmania)
